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Unlabelled: Estrogen is involved in ovarian cancer etiology. Crosstalk exists between estrogen and progesterone ending with the inhibition of estrogen effects. While estrogen induces ovarian cancer cell proliferation, progesterone protects women from ovarian cancer. The placenta facilitates estrogen and progesterone production. Moreover, during pregnancy epithelial ovarian cancer is more common than in young non-pregnant women and borderline ovarian tumors exhibit aggressive behavior These data suggest that pregnancy changes ovarian cancer characteristics., Aim: Analyzing the effect of placental soluble factors and estrogen+progesterone [E+P, in placental supernatant level) on epithelial ovarian cancer cell phenotype., Methods: Ovarian epithelial cancer cells (OVCAR-3, SKOV-3) were exposed to 1) supernatants collected from first trimester human placental explant culture; 2) E+P in levels equivalent to those measured in the placental supernatants. As a control OVCAR-3 and SKOV-3 were exposed to their supernatants or to the hormones solvent. Then we tested ovarian cancer cells proliferation, death, cell-cycle and migration., Results: Placental supernatants facilitated cancer cells migration and SKOV-3 proliferation. E+P facilitated SKOV-3 migration and elevated OVCAR-3 cell-number and apoptotic rate., Conclusion: Placental soluble factors and E+P affect ovarian cancer cells phenotype. Discussion: The elevated aggressiveness observed following exposure of ovarian cancer cells to placental supernatant and to E+P may contribute to the special phenomena observed in ovarian cancer during pregnancy. During pregnancy, ovarian cancer is usually discovered at an early stage, which improves patients' prognosis. Nevertheless, our results suggest that physicians should closely follow ovarian tumors during pregnancy as they might be affected by pregnancy-related factors.

The possible association between thyroid hormones and cancer has been reported over the years in pre-clinical and clinical studies. These studies suggest that high levels of hormones induce cancer cell proliferation while low levels slow disease progress. A context in which to interpret such findings is the recent description of a plasma membrane receptor for the thyroid hormone on cancer cells and dividing tumor-associated endothelial cells.